Brain dynamics supporting lexical retrieval after left hemisphere stroke This proposal examines the brain dynamics supporting lexical retrieval in patients with chronic stroke-induced aphasia due to left-hemisphere (LH) lesions. Patients presenting with stroke-induced aphasia due to LH damage often experience major lexical retrieval difficulties. Lexical retrieval abilities are, however, not equally compromised in these patients. One possible explanation for this variability is that lexical retrieval requires multiple cognitive components that are subserved by different neural regions. In particular, patients with lesions to the left lateral prefrontal cortex (LPFC) can often immediately recognize the word they are trying to say when given a choice between a few options or the onset of the target word. Patients with lesions in the left posterior temporal cortex (pLTC) may have trouble recognizing the correct word even when it is given to them. The LPFC and pLTC may therefore play different roles in subprocesses of lexical retrieval, lexical activation and selection, and brain network reorganization may consequently be different after LPFC versus pLTC stroke- induced lesions. Domain-general cognitive control processes have been proposed to play a role in recovery from stroke-induced aphasia. However, the degree to which domain-general cognitive control mechanisms are engaged in lexical retrieval following LH stroke is unclear. This project seeks to shed light on these issues. In particular, the proposed research will examine the spatio-temporal dynamics supporting lexical retrieval following LH stroke when lesions encompass the LPFC versus the pLTC, and how domain-general cognitive control may be engaged. Our main hypothesis is that patients with lesions encompassing the LPFC but not the pLTC will show more efficient engagement of domain-general cognitive control mechanisms in lexical retrieval than patients with lesions encompassing the pLTC. A combination of novel theoretical and methodological approaches will be used along with well-established tasks that assess lexical retrieval and domain-general cognitive control. Aim 1 will investigate the impact of damage to the LPFC versus pLTC on lexical retrieval to infer the causal roles of these regions in lexical activation and selection using established and novel behavioral modeling. Aim 2 will determine if and when domain-general cognitive control PFC regions are involved in lexical retrieval in patients with LPFC or pLTC lesions in comparison with matched-controls using spatially-enhanced scalp electroencephalography (EEG). Finally, Aim 3 will examine if differences in lexical retrieval abilities between these groups are subserved by differences in brain connectivity using EEG-derived functional connectivity measures. The personal and societal cost caused by lexical retrieval disruption after stroke is considerable. The results of these studies will provide a key step toward understanding brain dynamics supporting lexical retrieval in stroke-induced aphasia. These results may in turn lead to clinical tools for the assessment of lexical retrieval abilities.